Novel evidence that nitric oxide of the medial septal area influences the salivary secretion induced by pilocarpine

Our studies have focused on the effect of injection of L-NAME and sodium nitroprussiate (SNP) on the salivary secretion, arterial blood pressure, sodium excretion and urinary volume induced by pilocarpine which was injected into the medial septal area (MSA). Rats were anesthetized with urethane (1.25 g/kg b. wt.) and a stainless steel cannula was implanted into their MSA. The amount of saliva secretion was studied over a five-minute period after injection of pilocarpine into MSA. Injection of pilocarpine (10, 20, 40, 80, 160 mug/mul) into MSA produced a dose-dependent increase in salivary secretion. L-NG-nitro arginine methyl-esther (L-NAME) (40 mug/mul), a nitric oxide (NO) synthase inhibitor, was injected into MSA prior to the injection of pilocarpine into MSA, producing an increase in salivary secretion due to the effect of pilocarpine. Sodium nitroprussiate (SNP) (30 mug/mul) was injected into MSA prior to the injection of pilocarpine into MSA attenuating the increase in salivary secretion induced by pilocarpine. Medial arterial pressure (MAP) increase after injections of pilocarpine into the MSA. L-NAME injected into the MSA prior to injection of pilocarpine into MSA increased the MAP. SNP injected into the MSA prior to pilocarpine attenuated the effect of pilocarpine on MAP. Pilocarpine (40 mug/mul) injected into the MAS induced an increase in sodium and urinary excretion. L-NAME injected prior to pilocarpine into the MSA increased the urinary sodium excretion and urinary volume induced by pilocarpine. SNP injected prior to pilocarpine into the MSA decreased the sodium excretion and urinary volume induced by pilocarpine. All these roles of pilocarpine depend on the release of nitric oxide into the MSA. We may also conclude that the MSA is involved with the cholinergic excitatory mechanism that induce salivary secretion, increase in MAP and increase in sodium excretion and urinary volume. (C) 2002 Elsevier B.V. All rights reserved.

Lesions of the lateral hypothalamus impair pilocarpine-induced salivation in rats

In the present study we investigated the effects of electrolytic lesions of the lateral hypothalamus (LH) in the salivation induced by intracerebroventricular (i.c.v.) or intraperitoneal (i.p.) injection of the cholinergic agonist pilocarpine. Rats with sham or LH lesions and stainless steel cannulas implanted into the lateral ventricle (LV) were used. In rats anesthetized with urethane (1.25 mg/kg of body weight) saliva was collected using pre-weighed cotton balls inserted in the animal mouth during a period of 7 min following i.c.v. or i.p. injection of pilocarpine. Injection of pilocarpine (1 mg/kg of body weight) i.p. in sham-operated rats (6 h, 2, 7, and 15 days after the surgery) induced salivation (497+/-24, 452+/-26, 476+/-30, and 560+/-75 mg/7 min, respectively). The effects of i.p. pilocarpine was reduced 6 h, 2 and 7 days after LH lesions (162+/-37, 190+/-32, and 229+/-27mg/7 min, respectively), not 15 days after LH lesions (416+/-89mg/7 min). Injection of pilocarpine (120 mug/mul) i.c.v., in sham-operated rats (6 h, 2, 7, and 15 days after the surgery) also produced salivation (473 20, 382 16, 396 14, and 427 47 mg/7 min, respectively). The salivation induced by i.c.v. pilocarpine was also reduced 6 h, 2 and 7 days after LH lesions (243+/-19, 278+/-24, and 295+/-27 mg/7 min, respectively), not 15 days after LH lesions (385 48 mg/7 min). The present results show the participation of the LH in the salivation induced by central or peripheral injection of pilocarpine in rats, reinforcing the involvement of central mechanisms on pilocarpine-induced salivation. (C) 2002 Elsevier B.V. All rights reserved.

Involvement of central alpha(1)- and mu(2)-adrenoceptors on cardiovascular responses to moxonidine

In the present study we compared the effects produced by moxonidine (alpha(2)-adrenoceptor/imidazoline agonist) injected into the 4th cerebral ventricle and into the lateral cerebral ventricle on mean arterial pressure, heart rate and on renal, mesenteric and hindquarter vascular resistances, as well as the possible action of moxonidine on central alpha(1)- or alpha(2)-adrenoceptors to produce cardiovascular responses. Male Holtzman rats (n = 7-8) anesthetized with urethane (0.5 g/kg, intravenously - i.v.) and alpha-chloralose (60 mg/kg, i.v.) were used. Moxonidine (5, 10 and 20 nmol) injected into the 4th ventricle reduced arterial pressure (-19 +/- 5, -30 +/- 7 and -43 +/- 8 mmHg vs. vehicle: 2 +/- 4 mmHg), heart rate (-10 +/- 6, - 16 +/- 7 and -27 +/- 9 beats per minute - bpm, vs. vehicle: 4 +/- 5 bpm), and renal, mesenteric and hindquarter vascular resistances. Moxonidine (5, 10 and 20 nmol) into the lateral ventricle only reduced renal vascular resistance (-77 +/- 17%, - 85 +/- 13%, -89 +/- 10% vs. vehicle: 3 +/- 4%), without changes on arterial pressure, heart rate and mesenteric and hindquarter vascular resistances. Pre-treatment with the selective alpha(2)-adrenoceptor antagonist yohimbine (80, 160 and 320 nmol) injected into the 4th ventricle attenuated the hypotension (-32 +/- 5, -25 +/- 4 and -12 +/- 6 mmHg), bradycardia (-26 +/- 11, -23 +/- 5 and -11 +/- 6 bpm) and the reduction in renal, mesenteric and hindquarter vascular resistances produced by moxonidine (20 nmol) into the 4th ventricle. Pretreatment with yohimbine (320 nmol) into the lateral ventricle did not change the renal vasodilation produced by moxonidine (20 nmol) into the lateral ventricle. The alpha(1)-adrenoceptor antagonist prazosin (320 nmol) injected into the 4th ventricle did not affect the cardiovascular effects of moxonidine. However, prazosin (80, 160 and 320 nmol) into the lateral ventricle abolished the renal vasodilation (-17 +/- 4, -6 +/- 9 and 2 +/- 11%) produced by moxonidine. The results indicate that the decrease in renal vascular resistance due to moxonidine action in the forebrain is mediated by alpha(1)-adrenoceptors, while the cardiovascular effects produced by moxonidine acting in the brainstern depend at least partially on the activation of coadrenoceptors. (c) 2007 Elsevier B.V. All rights reserved.

Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine

Peripheral treatment with the cholinergic agonist pilocarpine induces intense salivation that is inhibited by central injections of the alpha(2)-adrenergic/imidazoline receptor agonist moxonidine. Salivary gland blood flow controlled by sympathetic and parasympathetic systems may affect salivation. We investigated the changes in mean arterial pressure (MAP) and in the vascular resistance in the submandibular/sublingual gland (SSG) artery, superior mesenteric (SM) artery and low abdominal aorta (hindlimb) in rats treated with intraperitoneal (i.p.) pilocarpine alone or combined with intracerebroventricular (i.c.v.) moxonidine. Male Holtzman rats with stainless steel cannula. implanted into lateral ventricle (LV) and anesthetized with urethane were used. Pilocarpine (4 mumol/kg of body weight) i.p. reduced SSG vascular resistance (-50 +/- 13% vs. vehicle: 5 +/- 3%). Pilocarpine i.p. also increased mesenteric vascular resistance (15 +/- 5% vs. vehicle: 2 +/- 3%) and MAP (16 +/- 3 mmHg, vs. vehicle: 2 +/- 3 mmHg). Moxonidine (20 nmol) i.c.v. increased SSG vascular resistance (88 +/- 12% vs. vehicle: 7 +/- 4%). When injected 15 min following i.c.v. moxonidine, pilocarpine i.p. produced no change on SSG vascular resistance. Pilocarpine-induced pressor responses and increase in mesenteric vascular resistance were not modified by i.c.v. moxonidine. The treatments produced no change in heart rate (HR) and hindlimb vascular resistance. The results show that (1) i.p. pilocarpine increases mesenteric vascular resistance and MAP and reduces salivary gland vascular resistance and (2) central moxonidine increases salivary gland vascular resistance and impairs pilocarpine-induced salivary gland vasodilatation. Therefore, the increase in salivary gland vascular resistance may play a role in the anti-salivatory response to central moxonidine. (C) 2003 Elsevier B.V. All rights reserved.

Cardiovascular responses to hydrogen peroxide into the nucleus tractus solitarius

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Important GABAergic mechanism within the NTS and the control of sympathetic baroreflex in SHR

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Inhibition of the caudal pressor area reduces cardiorespiratory chemoreflex responses

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Ventrolateral medulla mechanisms involved in cardiorespiratory responses to central chemoreceptor activation in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Chemosensory control by commissural nucleus of the solitary tract in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Involvement of the Central Nervous System in the Salivary Secretion Induced by Pilocarpine in Rats

The effect in rats of an anteroventral third ventricle (AV3V) electrolytic lesion on salivary secretion induced by intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) injection of a cholinergic agonist (pilocarpine) was investigated. Sham- or AV3V-lesioned rats anesthetized with urethane and with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The amount of salivary secretion was studied over a seven-minute period after i.c.v. or i.p. injection of pilocarpine. In sham-operated rats, i.p. injection of pilocarpine (1 mg/kg b.w.) (after 6 h, 2, 7, and 15 days) produced salivary secretion (486 +/- 21, 778 +/- 85, 630 +/- 50, and 560 +/- 55 mg/7 min, respectively). This effect was reduced 6 h, 2, and 7 days after an AV3V lesion (142 +/- 22, 113 +/- 32, and 290 +/- 62 mg/7 min, respectively), but not 15 days after an AV3V lesion (516 +/- 19 mg/7 min). I.c.v. injection of pilocarpine (120 mug in 1 muL), in sham-operated rats after 6 h, 2, 7, and 15 days also produced salivary secretion (443 +/- 20, 417 +/- 81, 496 +/- 14, and 427 +/- 47 mg/7 min, respectively). The effects of i.c.v. pilocarpine were also reduced 6 h, 2, and 7 days after an AV3V lesion (143 +/- 19, 273 +/- 14, and 322 +/- 17 mg/7 min, respectively), but not after 15 days (450 +/- 28 mg/7 min). The results demonstrate that the central nervous system, and particularly the AV3V region, is important for the effect of pilocarpine on salivary secretion in rats. Moreover, they suggest that activation of central pathways may play an important part in the salivary secretion to peripheral pilocarpine in rats.

Local structure and near-infrared emission features of neodymium-based amine functionalized organic/inorganic hybrids

Nd3+-based organic/inorganic hybrids have potential application in the field of integrated optics. Attractive sol-gel derived di-urea and di-urethane cross-linked poly (oxyethylene) (POE)/siloxane hybrids (di-ureasils and di-urethanesils, respectively) doped with neodymium triflate (Nd(CF3SO3)(3)) were examined by Fourier transform mid-infrared (FT-IR), Raman (FT-Raman), Si-29 magic-angle spinning (MAS) nuclear magnetic resonance (NMR) and photoluminescence spectroscopies, and small-angle X-ray scattering (SAXS). The goals of this work were to determine which cation coordinating site of the host matrix (ether oxygen atoms or carbonyl oxygen atoms) is active in each of the materials analyzed, its influence on the nanostructure of the samples and its relation with the photoluminescence properties. The main conclusion derived from this study is that the hydrogen-bonded associations formed throughout the materials play a major role in the hybrids nanostructure and photoluminescence properties.

A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Full-color phosphors from amine-functionalized crosslinked hybrids lacking metal activator ions

Sol-gel derived hybrids that contain OCH2CH2 (polyethylene glycol, PEG) repeat units grafted onto a siliceous backbone by urea, -NHC(=O)NH-, or urethane, -NHC(=O)O-, bridges have been prepared. It is demonstrated that the white light PL of these materials results from an unusual convolution of a longer lived emission that originates in the NH groups of the urea/urethane bridges with shorter lived electron-hole recombinations occurring in the nanometer-sized siliceous domains. The PL efficiencies reported here (maximum quantum yields at room temperature of ≈ 0.20 ± 0.02 at a 400 nm excitation wavelength) are in the same range as those for tetramethoxysilane-formic acid, and APTES-acetic acid, sol-gel derived phosphors. The high quantum yields combined with the possibility of tuning the emission to colors across the chromaticity diagram present a wide range of potential applications for these hybrid materials.

Haemodynamic effects of hypothalamic disconnection in anaesthetized rats

The aim of the present study was to analyse the haemodynamic effects induced by the hypothalamic disconnection (HD) caudal or rostral to the paraventricular nucleus of the hypothalamus (PVN). Mean arterial pressure (MAP), hindlimb, renal and mesenteric blood flow and vascular conductance (HVC, RVC and MVC, respectively) were measured in urethane (1.2 g/kg, i.v.) anesthetized rats for 60 min after disconnection. HD caudal to the PVN was performed with a double-edged microknife of bayonet shape (R=1 mm, H=2 mm) stereotaxically placed, lowered 2.8 mm caudal to the bregma along the midline. The cut was achieved by rotating the microknife 90° right and 90° left. HD rostral to the PVN was performed with the knife placed 0.8 mm caudal to the bregma. Thirty minutes after the hypothalamic disconnection caudal (HD-C), a decrease in MAP was observed (-14±3 mm Hg), reaching a 60-min decrease of 30±3 mm Hg. Hindlimb conductance increased 10 min after HD (156±14%) and remained elevated throughout the experimental period. On the contrary, we observed a transitory renal vasoconstriction (82±9%, ≤20 min) and a late mesenteric vasodilation, starting at 30 min (108±4%) and reaching 138±6% at 60 min. In rats with HD rostral to the PVN, we only observed minor changes in the cardiovascular parameters. In the MAP, there was a slight decrease 60 min after the hypothalamic disconnection rostral (HD-R) (-9±4 mm Hg). There were no significant changes in HVC. RVC and MVC were increased 60 min after the HD-R (116±12% and 124±11%, respectively). These results suggest that vasodilation in the hindlimb and in the mesenteric bed could contribute to the observed decrease in MAP in HD caudal to PVN rats. © 2002 Elsevier Science B.V. All rights reserved.

Degree of conversion of polymer-matrix composite assessed by FTIR analysis

Aims and objectives: The behavior of polymer-matrix composite is dependent on the degree of conversion. The aim of this study was to evaluate the degree of conversion of two resin cements following storage at 37°C immediately, 24 and 48 hours, and 7 days after light-curing by FTIR analysis. Materials and methods: The specimens were made in a metallic mold and cured with blue LED with power density of 500 mW/cm2 for 30 seconds. The specimens were pulverized, pressed with KBr and analyzed with FTIR following storage times. Statistical analysis used: ANOVA (two-way) and Tukey's post hoc. Results: To the polymer-matrix composites between 24 and 48 hours does not show a significant increase (p > 0.05), however, the highest values were found after 7 days. Conclusion: The polymer-matrix composites used in this study showed similarity on the degree of conversion and increased of according to the time of storage.